Antiangiogenic Drugs Are Stopping Neovascularization in Wet Macular Degeneration

(Updated 3/12/22)

A substance in the body called Vascular Endothelial Growth Factor (VEGF) is responsible for the growth of new blood vessels. It promotes this growth by stimulating the endothelial cells, which form the walls of the vessels and transport nutrients and oxygen to the tissues. Evidence shows that when the retinal pigment epithelial (RPE) cells begin to wither from lack of nutrition (a condition called “ischemia”), the VEGF goes into action to create new vessels. This process is called “neovascularization,” and it acts as a restorative function in other parts of the body. In the retina, however, the vessels do not form properly, and leaking results. This leakage causes scarring in the macula and eventual loss of central vision.

Antiangiogenic drugs prevent the VEGF from binding with the receptors on the surface of the endothelial cells. In most cases, the drugs are injected into the vitreous of the eyeball, then pass into the subretinal space, where the vessels proliferate. Neovascularization is then blocked, preventing bleeding into the retina.

New research is looking for less invasive and burdensome introduction of the drugs by way of topical eye drops, implanted timed release capsules, and implanted ports of delivery. The most recent breakthrough is FDA approval of Susvimo. This procedure continuously delivers a form of ranibizumab (Lucentis), offering an alternative to anti-VEGF eye injections. The tiny implant is surgically inserted into the eye during a one-time outpatient procedure and refilled every six months. More about Susvimo.
Here is information on current anti-angiogenic drugs being studied or already being used in the clinics:

In clinic use:
Macugen (pegaptanib sodium) [approved 2004]
Lucentis (ranibizumab) [approved 2006]
EYLEA (aflibercept) [approved 2011]
Avastin (bevacizumab) [available off-label since 2007]
Brolucizumab (RTH-258) [approved 2019]
Byooviz (ranibizumab-nuna) [approved 2021]
Faricimab (Vabysmo) [approved 2022]

Under study:
AKST4290 (oral)
X-82 (oral)

Macugen (pegaptanib sodium)
Macugen, made by OSI EyeTech Pharmaceuticals, was the first antiangiogenic drug to gain FDA approval. Pegaptanib is a chemically synthesized strand of genetic material that bonds with VEGF cells to block replication. A large trial of Macugen on 1,196 patients at 117 centers around the world was completed in 2003. In November of that year, data presented to the American Academy of Ophthalmology (AAO) showed that Macugen stabilized or improved vision in 33% of the patients in the trials, while the same results occurred in 23% of a control group not given Macugen. As many as 71% of the patients given Macugen lost less than three lines of vision during the year, compared with 55% in the control group. The drug is injected directly into the eye every six weeks, or about nine times a year.
Working in conjunction with Pfizer Ophthalmics, Macugen gained FDA approval on December 17, 2004, and was ready for public use beginning in 2005.

Genentech, Inc. announced on May 23, 2005 that a Phase III clinical study of the investigational drug Lucentis (ranibizumab) met its primary efficacy endpoint of maintaining vision in patients with wet AMD. Approximately 95 percent of patients maintained or improved vision (defined as a loss of less than 15 letters in visual acuity) at one year when treated with Lucentis injections compared to approximately 62 percent of those treated in the control arm. Vision improvement was an unexpected result that had not been seen at a significant level in other antiangiogenic drug trials. Lucentis is approved for use in the European Union, Switzerland, India, Canada and the United States. A regulatory decision in Australia is expected before the end of 2007.
On January 14, 2006, one-year data from the second pivotal Phase III study of Lucentis were presented at the Macula 2006 meeting in New York. Data showed that, for the second time in a large, Phase III study, Lucentis improved vision in patients with wet AMD.
On November 13, 2006, several new findings were presented at the 2006 AAO meeting:
Elias Reichel, M.D. reported that in the MARINA trials, there was improvement at all visual acuity levels, but there was not a big difference if the patient’s baseline vision was either low or excellent. This “floor-to-ceiling” effect is not unusual with this kind of study, but it is useful information for patient communicating with patients about expectations.
Nancy Holekamp, M.D., discussed key anatomic endpoints in the MARINA trials, in particular, the total lesion area over time (no growth of the lesion area was noted in the treated patients), the mean area of leakage (the amount of decrease was statistically significant) and the mean foveal retinal thickness (treated eyes showed a significant thinning of the retina). The bottom line is that all anatomic outcomes from the trial favored Lucentis, and the treatment is so effective over a long period of time without any signs of toxicity, there is no indication that anything in lieu of Lucentis should be used to treat wet AMD.
Peter Kaiser, M.D., reported on subgroup analysis of Genentech’s PIER study. The primary endpoint was met, showing a difference of 16 letters visual acuity between the treated group and the sham group. Further, the dosing regimen was effective, but the visual acuity benefit was not as robust when injections went from monthly to quarterly. The persistence of monthly injections may depend upon who has dry lesions and who has wet lesions at the 5th month. The dry lesion group did better than the wet lesion group with quarterly dosing. This data is pointing toward better prediction of dosage outcomes for individual patients.
On February 15, 2007, Dr. Kaiser reported two-year results of the Phase 3 ANCHOR trial comparing Lucentis with photodynamic therapy (PDT) for wet AMD. The study showed that Lucentis helps maintain vision, with few adverse effects, significantly better than PDT. 89.9% of patient randomised to Lucentis in a head-to-head comparison with Visudyne for photodynamic therapy (PDT) lost fewer than 15 letters on a visual acuity chart at 24 months compared to 65.7% of those treated with PDT. 78% of the Lucentis-treated group maintained their baseline visual acuity or gained letters, compared to only 29% of the PDT group. Overall, patients randomised to Lucentis had a 20.5 letter benefit at 24 months (+10.7 EDTRS letters) compared to those treated with PDT (-9.8 letters). This was similar to visual acuity seen at 12 months (+11.3 letters with Lucentis vs -9.6 letters with PDT).
On February 23, 2008, the final results from Cohort 1 of the Phase IIIb SAILOR study of Lucentis in patients with wet AMD were presented on February 23, 2008 at the Bascom Palmer Eye Institute’s Angiogenesis meeting by Dr. David Boyer (Retina-Vitreous Associates Medical Group, Los Angeles). The final, one-year data support the long-term safety and efficacy profile of Lucentis.
The study, titled “Ranibizumab (Lucentis) Safety in Previously Treated and Newly Diagnosed Patients with Neovascular Age-related Macular Degeneration (AMD): The SAILOR Study,” was designed to evaluate the safety of two different doses of Lucentis (0.5 mg, the FDA-approved dose, and 0.3 mg) administered once a month for three months and thereafter as needed based on re-treatment criteria.
For more detail in all of these areas of study, see

EYLEA (aflibercept injection, formerly VEGF Trap-Eye)
In August 2008, Regeneron Pharmaceuticals, Inc. and Bayer HealthCare AG announced that patients with wet AMD receiving EYLEA (aflibercept injection) in a Phase 2 extension study on an “as needed” dosing schedule continued to show highly significant improvements in retinal thickness and vision gain at 52 weeks. There were no drug-related serious adverse events, and treatment was generally well-tolerated.
For all dose cohorts combined, there was a 5.3 mean letter gain in visual acuity at the end of 52 weeks. The mean decrease in retinal thickness was 130 microns versus baseline. During weeks 12 to 52, patients from all dose groups combined received, on average, only two additional injections. This supported Regeneron’s expectation that, with EYLEA treatment, patients’ visual acuity would improve over time without the need for monthly intravitreal injections.
A phase 3 study, VIEW 1, began enrolling patients in late 2007. The VIEW 1 study compared EYLEA and Lucentis. A phase 2 study in diabetic macular edema (DME) was also completed. EYLEA injected into the eye every two months was found to be as effective as monthly doses of Lucentis, and monthly monitoring of patients receiving EYLEA was not necessary.
On June 17, 2011, the Food and Drug Administration advisory panel voted unanimously to recommend EYLEA as a treatment for wet AMD. The advisers also said the injected drug could be given once every two months. This was an improvement upon the typical 4-6 week dosings of both Lucentis and Avastin.
Finally, on November 18, 2011, Regeneron announced that the FDA had approved EYLEA for treatment of patients with wet AMD. Recommended dose is 2 mg every four weeks for the first 12 weeks, followed by 2 mg every eight weeks. EYLEA offers less frequent injections than either Lucentis (4 weeks) or Avastin (6 weeks), and there are no monitoring requirements.
Since September 2012, Eylea has also gained approval in the U.S., Europe, and Japan for use in treating wet AMD, diabetic macular edema, and neovascular myopic degeneration. For more information, see

Avastin (bevacizumab)
Avastin (bevacizumab), has been shown in preliminary off-label studies to stop blood vessel growth and leakage in the retinas of patients with macular degeneration. Testing began in March 2005 at the Bascom Palmer Eye Institute in Miami under the leadership of Dr. Philip Rosenfeld. In July 2005, Dr. Peter Campochiaro followed with subjects at the Johns Hopkins Medical Center in Baltimore. Potential side effects, according to Rosenfeld, are increased risk of stroke or heart attack in patients taking chemotherapy, and elevation of blood pressure. Systemic infusions of Avastin, he said would be needed every few months.
On February 15, 2007, Elias Reichel, M.D. reported to Hawaiian Eye/Retina 2007 that Avastin has shown good results in a small retrospective case series for treatment of neovascularization from myopic degeneration. 15 eyes studied showed a mean improvement in acuity of 3 lines, central foveal thickness decreased an average of 93 micrometers and no complications.
In May 2011, first year results of the Comparison of AMD Treatments Trial (CATT) were announced. The report focused on the relative safety and efficacy of Lucentis and Avastin. After one year, the two compounds have been found to be extremely similar in their improvement of mean visual acuity and the occurrence of adverse events. Five related trials were also undertaken in the UK and Europe.
At the end of the 2-year comparison study, The National Institutes of Health reported that both drugs improved vision when administered monthly or on an as needed basis. Patients receiving Lucentis, however, fully maintained first-year vision gains with an average 5.7 injections in the second year. In contrast, patients treated with Avastin experienced a greater decline in vision despite receiving significantly more injections over the two year period. In addition, secondary anatomical outcomes were significantly better with Lucentis. For more information, see

Faricimab (Vabysmo)
A global Phase III program for faricimab in wet AMD began in 2019. The efficacy of faricimab administered at 12- and 16-week intervals was evaluated against ranibizumab every 4 weeks. At week 24, researchers reported in May 2020 that 65% of faricimab-treated patients were disease activity-free. By January 2021, further research had shown that people receiving faricimab injections at fixed intervals of up to every 16 weeks achieved visual acuity outcomes as effective as those receiving Regeneron’s aflibercept (Eylea) injections every eight weeks. More information.

PAN-90806 is a topical eye drop for the treatment of neovascular AMD, diabetic retinopathy, and potentially diabetic macular edema (DME). It is being developed by Panoptica and began a phase 1 clinical trials in early 2014, a 2-month open-label study of approximately 30 patients at 15 to 20 sites in the U.S. The study was completed in May 2016. More information.

OPT-302 is soluble receptor developed by Opthea Pty Ltd. It is a derivative of VGX-300 which has been optimised for local ocular administration. OPT-302 potently and specifically blocks VEGF-C and VEGF-D from binding and activating VEGFR-2 and VEGFR-3.
On August 6, 2019, Opthea announced positive Phase 2b results demonstrating that OPT-302 combination therapy showed improvements across multiple secondary endpoints at 24 weeks. Compared to Lucentis monotherapy, OPT-302 (2.0 mg) combination treatment showed improvements that included a higher proportion of patients with stable vision (defined as ≤ 15 letter loss from baseline), and those gaining ≥10 and ≥15 letters of visual acuity. On March 15, 2021, Opthea announced that, based upon the positive Phase 2 results, the first patient has now been enrolled in the Phase 3 trial. More information

The EMERGE study examined the hypothesis that a protein called Tissue Factor (TF), when out of control, initiates inflammation and angiogenesis, resulting in wet AMD. ICON-1 is thought to block the protein and reverse the progression of the disease, both alone and in combination with Lucentis.
Phase 2a results showed that ICON-1 was well tolerated and that in combination with anti-VEGF therapy treated both the symptoms and the underlying process driving inflammation and CNV. The combination effectively reduced CNV lesion size, increased the durability of effect and improved removal of pathologic fluid from the retina. Based on these positive results, the company initiated a Phase 2b study of ICON-1 in combination with anti-VEGF treatment in 2018. More information

Regenxbio’s RGX-314 differs from current therapeutics in that it includes a gene vector (NAV AAV8) which encodes an antibody fragment designed to neutralize VEGF (vascular endothelial growth factor) activity. This modifies the pathway for formation of new leaky blood vessels which lead to retinal fluid accumulation and vision loss.
In August 2019, Regenxbio reported positive phase 1/2a results in patients with wet age-related macular degeneration, and that the drug is continuing to be well tolerated across five dose cohorts.
Investigation of RGX-314 with a phase IIb trial (AAVIATE) is proceeding, with dosing of the first patient using suprachoroidal delivery. As of December 31, 2020, suprachoroidal delivery of RGX-314 was reported to be generally well-tolerated, with no evidence of inflammation.

More information

Brolucizumab (RTH258)
Novartis announced on October 8, 2019 that the US Food and Drug Administration (FDA) approved BEOVU® (brolucizumab-dbll) injection for the treatment of wet age-related macular degeneration (wet AMD).  BEOVU® carries a recommended dosing schedule of monthly for the first three doses followed by one dose every 8-12 weeks. More information.

Allergan trials have demonstrated that the biological drug Abicipar is equal to Genentech’s Lucentis (ranibizumab), with the added benefit that Abicipar treatments are effective at up to 12-week dosages. This is longer than Lucentis (4 weeks), Avastin (6 weeks), and Eylea (8 weeks), the three currently available drugs for treatment of wAMD. Trials are ongoing. More information

Kodiak trials showed good results for treatment of diabetic macular edema. Twelve weeks after a single dose of KSI-301 saw improvement of almost two lines (9 eye chart letters) and retinal edema of 121 microns. Unfortunately, Phase 3 results showed that, although KSI-301 demonstrated strong durability and was safe and well tolerated, it did not meet the primary efficacy endpoint of showing non-inferior visual acuity gains for subjects dosed on extended regimens compared to aflibercept given every eight weeks. More information.

Graybug Vision’s novel investigational depot approach is designed to continuously inhibit activity of all VEGF receptors for the treatment of wet AMD. In Phase 1 trials, GB-102 was well-tolerated with no dose limiting toxicities, drug-related serious adverse events or inflammation. 88% and 68% percent of evaluable patients were maintained only on a single dose of GB-102 at 3- and 6-months, respectively. Patients with wet-AMD require intravitreal injections every 6 to 8 weeks, on average, with the current standard-of-care.

Graybug Vision’s Phase 2b ALTISSIMO study of GB-102, was completed in January 2021. Topline data are expected to be announced in the second quarter of this year, and full results presented in the later part of 2021 at a medical conference.

Graybug announced in April 2022 that it plans to proceed with a Phase 2 clinical trial of an optimized formulation of GB-102 in wet AMD patients following successful demonstration of improved performance in an extensive battery of novel in vitro stress tests. This decision, supported by a significantly more favorable competitive landscape following recent readouts of other long-acting vascular endothelial growth factor (VEGF) inhibitors, is anticipated to result in a six-month data readout available in the third quarter of 2023.

More information

X-82 (Oral)
Under study by Tyrogenex, Inc., this oral medication is intended for use in combination with anti-VEGF injections. The expectation is that the combination therapy will reduce the number of injections required for stabilizing the retina. Phase 2 trials began in 2017. More information.

AKST4290 (Oral)
Alkahest Inc. has reported that AKST4290, an oral medication for treatment of wet AMD, was shown in trials to be safe, effective, and “extremely promising”. Two Phase 2a clinical trials for AKST4290 were recently completed: one in naïve patients and one in refractory wet AMD patients. Results are pending. More information

In April 2019, Innovent Biologics announced that it had dosed the first patient in a phase 1 trial of IBI302, the company’s wet AMD treatment candidate. A single intravitreal injection of IBI302, a recombinant fully human bispecific fusion protein targeting VEGF and complement proteins, will be evaluated in 36 patients with wet AMD in the open-label, single-center, dose escalation clinical trial. More information


In August 2019,  Aerie Pharmaceuticals, Inc. (Aerie), began patient dosing in their first human clinical trial of a sustained release implant in patients with wet macular degeneration or diabetic macular edema. The polymer implant provides controlled release of AR-13503, an injectable drug that inhibits blood vessel growth in the retina, while potentially reducing the treatment burden associated with more frequent intravitreal injection. More information

RBM-007 is a novel oligonucleotide-based aptamer with potent anti-FGF2 (fibroblast growth factor 2) activity. A Phase 2 Study assessing the safety, efficacy and durability of RBM-007 is underway. More information

Byooviz (ranibizumab-nuna)
The first biosimilar to ranibizumab injection for wet AMD. Also approved to treat macular edema and myopic choroidal neovascularization. More information.

A potential twice-yearly sustained delivery intravitreal anti-VEGF treatment for wet age-related macular degeneration (wAMD). More information

IL-18 Can Prevent Inflammation in the Retina

by Dan Roberts
Updated April 2014
A new finding by researchers at Trinity College Dublin may lead to another treatment for wet AMD. Inflammation in the retina results from blood vessel development, and the natural component named IL-18 has been found to keep the process under control. By injecting the chemical into the eye, or by injecting a gene that produces IL-18, the scientists speculated that they could keep dry AMD from developing into wet AMD. In other words, it would be a preventative treatment, similar to a vaccination.
This discovery was the first step in a long road to clinical application. It must first be tested in animals, then go through human clinical trials, which means about 10 years of intensive lab work and fund raising. Co-authors of the Nature Medicine paper, published in the April 2012 issue of Nature, were Dr. Sarah Doyle and Dr. Matthew Campbell.
After 2 years of further study researchers reported online April 2, 2014 in Science Translational Medicine that that low doses of IL-18 had no adverse effects on the retina and yet still suppressed abnormal blood vessel growth. They also found that IL-18 seems effective when given intravenously instead of through injections directly into the eye.

siRNA Turns Off Bad Genes

by Dan Roberts
(updated April 2009)
A new type of anti-VEGF drug called “small interference RNA (siRNA),” is showing promise in its ability to turn off genes that cause wet AMD.
A preliminary primate study in early 2004 showed that, at the highest dose used in the study siRNA (formerly called RNAi) “reduced the incidence of clinically significant vascular leakage to zero by week three and for the duration of the study, and at day 35 neovascularization was inhibited by greater than 65 percent in the high dose group. No adverse effects were observed.” (“Intravitreal injection of VEGF siRNA Inhibits growth and leakage in a non-human primate laser induced model of CNV,” by Tolentino, et al., Retina, the Journal of Retinal and Vitreous Diseases, Feb 2004.)
Acuity Pharmaceuticals (Philadelphia, PA) has developed and begun testing on anti-VEGF (vascular endothelial growth factor) small interfering RNA labeled Cand5. In a phase 1 clinical trial, the safety and tolerability of Cand5 were evaluated in subjects who were all more than 70 years of age with predominantly classic, minimally classic and occult wet AMD. In a presentation to the American Academy of Ophthalmology (AAO) annual meeting, John Thompson, MD (Assistant Professor, Wilmer Eye Institute, Johns Hopkins University, Baltimore, Maryland) reported that Cand5 was found to be safe and well tolerated following repeated administration at escalating doses. As a result of these findings, a phase 2 trial was approved by the FDA.
New York Times writer Andrew Pollack provided a good explanation of how the process works (“Method to Turn Off Bad Genes Is Set for Tests on Human Eyes,” 9/14/04):
“RNA [ribonucleic acid] is a string of chemical units, called bases, that represent the letters of the genetic code. It serves as a messenger, carrying the recipe for a protein from the DNA in the genes to the cell’s protein-making machinery. Proteins form much of the structure of a cell and carry out much of its activities.
“While DNA has two strands (the double helix) RNA is usually single-stranded. If cells sense double-stranded RNA, they act to destroy it and any other RNA with the same sequence. Some researchers think that this RNA interference mechanism might have evolved as a defense against viruses, which sometimes create double-stranded RNA.
“Scientists can harness this mechanism to prevent any gene in the body from being used to make a protein, effectively shutting off the gene. They synthesize a short string of double-stranded RNA that corresponds to part of the messenger RNA carrying the protein recipe. Rather than creating the protein, the cell destroys the messenger.”
Other companies have demonstrated that wet AMD can be treated by blocking the action of VEGF, which causes the formation of leaking blood vessels. (See Antiangiogenic Drugs Are Stopping Neovascularization in Wet Macular Degeneration.) But instead of blocking the action of the protein, the siRNA approach turns off the gene, blocking the protein from being formed in the first place.
In a communication from Gislin Dagnelie, Ph.D. (Assistant Professor of Ophthalmology and Director of Low Vision Services, Lions Vision Research & Rehab Center, Johns Hopkins University School of Medicine), MD Support learned that siRNA therapy is especially important for dominant forms of retinitis pigmentosa (RP), “where the same mechanism could be applied in families with known [genetic] mutations.” Assuming that there are no significant side effects, he said, affected children could get such treatments, which would keep them from ever having any RP symptoms. The bad gene, however, could still be passed on to their children.
Dr. Dagnelie then offered a cautionary note: “Each genetic defect would require its own siRNA, and developing these treatments is not cheap, as separate safety and efficacy trials will be needed for each variant. But once a few of them have been shown [to be] safe and the mechanisms are all understood, the manufacturing and evaluation processes may be streamlined. This is very exciting, not just as a development in the fight against wet AMD, but as an example for other diseases where blocking the action of a bad gene could prevent most of the damage the disease causes.”
Initial clinical trials were conducted in Baltimore and Cleveland. Future studies will also be conducted in additional cities in the U.S. For information regarding the trials, contact Theresa Nicholson.
UPDATE 1: On November 13, 2006, John Thompson, M.D., reported to the 2006 AAO annual meeting that studies have found no significant difference in three dose levels of bevasiranib, Acuity’s siRNA drug under study. Results indicate that treatment with direct VEGF inhibitors may be necessary initially before treatment with bevasirinab. Hopefully, said Dr. Thompson, a Phase III study will show effectiveness of the drug as long term treatment.
UPDATE 2: In 2008, the journal Nature carried reports by Dr. Jayakrishna Ambati and colleagues, who found that siRNA is toxic to blood endothelial cells, which line blood vessels. Then, in April 2009, new findings were published in the online issue of Proceedings of the National Academy of Sciences. In concert with Sandro De Falco and Arturo Brunetti (Naples), Ambati et al found that siRNAs, by activating an immune receptor called toll-like receptor 3 (TLR3), also generically block blood and lymphatic vessel growth in muscle tissue as well. This indicates that siRNA may be utilized in the treatment of diseases of the lymphatic system, as well.

CD36 Deficiency May Cause Dry AMD

by Dan Roberts
February 2008
CD36 is a protein molecule (called an “integral membrane protein”) permanently attached to the surface of certain human cells. It plays a role in the inflammation process, but researchers have now discovered that a deficiency of the protein may cause the dry form of macular degeneration.
Researchers reported that deficiency of CD36 in rodent models led to significant progressive age-related photoreceptor degeneration. They think this is caused by a resulting down-regulation of COX2, an enzyme that is important to blood vessel formation. Uncontrolled blood vessel growth (neovascularization) is a hazard to the retina, as in wet AMD. A decrease, however, in the normal size and number of choroidal vessels will starve the photoreceptor cells, causing the dry form of the disease.
This discovery may lead to a treatment for CD36 deficiency, which could have important implications for the development of new therapies for dry AMD. The research was published on February 19, 2008 in PLoS Medicine (“CD36 Deficiency Leads to Choroidal Involution via COX2 Down-Regulation in Rodents,” Florian Sennlaub, et al, INSERM, Universite Pierre et Marie Curie, Paris).

SAILOR Study Results Favorable

by Dan Roberts
February 23, 2008
The final results from Cohort 1 of the Phase IIIb SAILOR study of Lucentis in patients with wet AMD were presented on February 23, 2008 at the Bascom Palmer Eye Institute’s Angiogenesis meeting by Dr. David Boyer (Retina-Vitreous Associates Medical Group, Los Angeles). The final, one-year data support the long-term safety and efficacy profile of Lucentis.
The study, titled “Ranibizumab (Lucentis) Safety in Previously Treated and Newly Diagnosed Patients with Neovascular Age-related Macular Degeneration (AMD): The SAILOR Study,” was designed to evaluate the safety of two different doses of Lucentis (0.5 mg, the FDA-approved dose, and 0.3 mg) administered once a month for three months and thereafter as needed based on re-treatment criteria. The top line results were:

  • Rates of ocular and non-ocular serious adverse events at one year were similar in patients receiving either 0.3 mg or 0.5 mg of Lucentis and consistent with previous studies, supporting the long-term safety of Lucentis
  • Rates of ocular and non-ocular adverse events at one year were generally low in both dose groups and consistent with previous studies.
  • One-year results also demonstrated that the FDA-approved dose of Lucentis (0.5 mg) was not associated with the higher rate of stroke observed during the planned interim analysis at six months.Ê The data suggested a trend towards a higher incidence of stroke in the 0.5 mg dose group (1.2% vs. 0.7% in the 0.3 mg group), though the results were not statistically significant (p-value=0.21).
  • At one-year, patients with a prior history of stroke had a higher rate of stroke in the 0.5 group (9.6%) compared to the 0.3 group (2.7%).Ê However, this trend was inconclusive, as the number of events was small. These data are consistent with epidemiologic data showing that prior history of stroke predisposes patients to subsequent stroke.

One-year SAILOR efficacy data suggested that treating patients with Lucentis on an as needed basis may be less effective than monthly dosing.